| Adenocarcinoma of pancreas is one of the most aggressive neoplasia, which is with atypical feature in clinical and low survival rate, and remains silent until late in its course. Highly abnormal chromosome karyotypes, including nonrandom pattern of which may be helpful for diagnosis and therapy to this tumor, must contribute to the genetic events that drive tumorigenesis and progression. The numerical and structural chromosomal aberrations from pancreatic cancer are very complex from the studies of past years. Specific chromosome abnormalities, which were revealed by cytogenetic analysis, especially including considerable new methods, may help in the diagnosis for familial pancreatic cancer and the treatment. Deletion of chromosome 9p,13q,17p and 18q, and gain of 7q,8q,12p,19q and 20q with highly frequency were observed by the most investigators.Although a lot of genetic data, including chromosome instability, were obtained past few years, the chromosome characteristic with relatively high accuracy in Chinese patients was not identified as our knowledge because of the limits of classical cytogenetic tools. On the basis of our previously relevant results on the pancreatic cancer using G-banding, chromosome painting and conventional FISH methods, we furthermore analyzed 5 cell lines of pancreatic cancer from Chinese patients we established, which are P1,P2,P3,P4, P7 and 1 cell line Panc-1 from ATCC, by spectral karyotyping (SKY), for exploring the nature of chromosome together with its' likely differences between ethnicities and the effects during tumorigenesis.Our results show that the chromosome instability in whole cell lines from pancreatic cancer, which involved 5 from Chinese and 1 from ATCC, happens in very high frequency, that include(1) very complex karyotype are revealed and the numerical and structural chromosomal aberrations refer to almost all of the metaphases evaluated for every cell lines are observed. Totally 175 chromosome changes which include hapotetraploid in Panc-1, hapotriploid in P1,P2, P3,P4, and hyperdiploid in P7, are identified. (2) Loss of chromosome (entire or part) is more common compare with gain of chromosome (entire or part). The gains involved chromosome 3,4,5,7,13,14,18 and 2O.The losses involved chromosome 1,3,4,5,8,9,11, 13,15,16,17,18,19,20,21,22,X and Y. The most common partial or whole arm gains affected 5p and 12q, etc. The most common partial or whole arm losses affected 10p,15p,16p,21p etc. We found some nonrandem chromosome structural aberrations in≥2 cell lines, which are der(9;15)(q10;q10) in P1,P2,P3,P4 and Panc-1;der(10)(3;10 )(?;q26) in P1,P2 and P3;der(12)(8;12)(?;p13)in P1,P2 and P4;del(5)(q22)in P2 and P3;del(8)(?)and der(12;18)(q10;p10)in PI and P3, as well as the losses of 10p in the all of 6 cell lines and 15p in the cell lines of P1,P2, P3 and P4 are found by us for the first time as far as we know.Our findings implied that it is very necessary for confirm the complex chromosome changes reveled in Chinese pancreatic cancer in more sources including tissue samples. It is worthwhile for further study on the most often events of-10p and-15p in our cohort, which is not reported before, for understanding the relationship between chromosome instability and pancreatic carcinogenesis and progression. |